Cell Autophagy in NASH and NASH-Related Hepatocellular Carcinoma

• Published in: International journal of molecular sciences Vol. 23; no. 14; p. 7734
• Main Authors: Udoh, Utibe-Abasi S., Rajan, Pradeep Kumar, Nakafuku, Yuto, Finley, Robert, Sanabria, Juan Ramon
• Format: Journal Article
• Language: English
• Published: Basel MDPI AG 13.07.2022; MDPI
• Subjects: Aging; Autoimmune diseases; Autoimmunity; Autophagy; cell autophagy; Cell differentiation; Differentiation (biology); Endoplasmic reticulum; Enzymes; Fatty liver; Hepatocellular carcinoma; Homeostasis; Hypertension; Inflammatory diseases; Insulin resistance; Kinases; Lipids; Liver cancer; Liver diseases; Lysosomes; Mammalian cells; Mammals; Metabolism; Microbiota; NASH; NASH-related HCC; Neurodegeneration; Organelles; Proteins; Quality control; Review; Steatosis
• ISSN: 1422-0067; 1661-6596; 1422-0067
• DOI: 10.3390/ijms23147734

Autophagy, a cellular self-digestion process, involves the degradation of targeted cell components such as damaged organelles, unfolded proteins, and intracellular pathogens by lysosomes. It is a major quality control system of the cell and plays an important role in cell differentiation, survival, development, and homeostasis. Alterations in the cell autophagic machinery have been implicated in several disease conditions, including neurodegeneration, autoimmunity, cancer, infection, inflammatory diseases, and aging. In non-alcoholic fatty liver disease, including its inflammatory form, non-alcoholic steatohepatitis (NASH), a decrease in cell autophagic activity, has been implicated in the initial development and progression of steatosis to NASH and hepatocellular carcinoma (HCC). We present an overview of autophagy as it occurs in mammalian cells with an insight into the emerging understanding of the role of autophagy in NASH and NASH-related HCC.